Taketani S, Kohno H, Yoshinaga T, Tokunaga R
Department of Hygiene, Kansai Medical University, Osaka, Japan.
FEBS Lett. 1989 Mar 13;245(1-2):173-6. doi: 10.1016/0014-5793(89)80215-7.
Exposure of HeLa and HL60 cells to sodium arsenite or cadmium chloride led to marked increases in cellular heme oxygenase activity. SDS-polyacrylamide gel electrophoresis of [35S]methionine-labeled cellular proteins indicated that these treatments also resulted in the induction of a 32-kDa protein. Immunoblot analysis further showed that the 32-kDa protein reacted with anti-bovine heme oxygenase antibodies. Treatment of the cells with cobaltic chloride or heat induced neither the 32-kDa protein nor heme oxygenase activity. It is concluded that the 32-kDa stress protein induced by arsenite and cadmium ions in these human cells is heme oxygenase.
将HeLa细胞和HL60细胞暴露于亚砷酸钠或氯化镉中会导致细胞血红素加氧酶活性显著增加。对用[35S]甲硫氨酸标记的细胞蛋白质进行SDS-聚丙烯酰胺凝胶电泳表明，这些处理还导致一种32 kDa蛋白质的诱导表达。免疫印迹分析进一步表明，这种32 kDa蛋白质与抗牛血红素加氧酶抗体发生反应。用氯化钴处理细胞或加热既不会诱导32 kDa蛋白质的产生，也不会诱导血红素加氧酶活性。得出的结论是，在这些人类细胞中由亚砷酸盐和镉离子诱导产生的32 kDa应激蛋白是血红素加氧酶。
